Redox Regulation in Inflammation and Disease—3rd Edition

A special issue of Antioxidants (ISSN 2076-3921).

Deadline for manuscript submissions: 20 October 2025 | Viewed by 337

Special Issue Editors


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Guest Editor
Department of Otorhinolaryngology, University Medicine Essen, Essen, Germany
Interests: redox regulation; signal transduction; TRX family proteins; (neuro-) inflammation; cell communication; tumor–stroma crosstalk; neutrophil biology; translational immunology
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Guest Editor Assistant
Cell Biology and Neuroscience “De Robertis” Institute (IBCN), Medical Faculty, University of Buenos Aires, Buenos Aires, Argentina
Interests: neurodegenerative diseases; axonal transport; redox regulation; mitochondrial homeostasis; TRX family proteins

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Guest Editor Assistant
Department of Dermatology and Allergology, Philipps-Universität Marburg, Marburg, Germany
Interests: autoimmunity; animal models; autoimmune bullous diseases; redox regulation; translational immunology

Special Issue Information

Dear Colleagues,

We differentiate between oxidative eu- and distress, recognizing the role of various factors such as i) the regulated enzymatic production and decay of specific reactive oxygen species (ROS), ii) their role as second messengers, and iii) the presence of regulatory thiol switches and their function in redox-mediated signaling.

Specific reactive species, including hydrogen peroxide, hydrogen sulfide, and nitric oxide, are essential for physiological processes including metabolism and signal transduction, as well as cell proliferation, differentiation, and death. Redox regulation of (membrane) proteins, enzymes, and transcription factors such as NFκB is crucial for the chemotaxis and activation of immune cells, the production and release of immune mediators, and cell communication within distinct physiological and pathological microenvironmental niches. Interestingly, extracellular redox proteins, low-molecular-weight thiols, and thiol switches can also affect signal transduction and cell communication.

Changes in the expression, protein levels, or distribution of specific redox proteins can be assessed using histological techniques. These changes have been associated with many disorders linked to ischemia and inflammation and more specifically to distinct subpopulations of immune cells.  Redox changes can be analyzed in body fluids and isolated immune cell populations without using invasive and expensive techniques, maintaining their potential for developing new preventive and diagnostic tools and innovative treatments.

For this Special Issue, we invite researchers to provide original research articles that report results combining the topics of redox regulation, inflammatory signaling, and translational immunology. We encourage studies that highlight the role of specific reactive species, redox proteins, and/or thiol switches. Additionally, we welcome clinical studies demonstrating significant changes in the levels or activities of i) redox proteins, ii) low-molecular-weight thiols, and/or iii) altered redox states of proteins in diseases linked to inflammation or neuroinflammation. Review articles discussing the current state of the art are also welcome.

Yours faithfully,

Dr. Eva-Maria Hanschmann
Guest Editor

Dr. Mariana Ines Holubiec
Dr. Christoph Hudemann
Guest Editor Assistants

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • redox signaling
  • reactive oxygen and nitrogen species
  • inflammation
  • signal transduction
  • thiol switches
  • regulation of immune cells
  • translational immunology

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Published Papers (1 paper)

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Review

31 pages, 966 KiB  
Review
Redox Imbalance in Inflammation: The Interplay of Oxidative and Reductive Stress
by Francesco Bellanti, Anna Rita Daniela Coda, Maria Incoronata Trecca, Aurelio Lo Buglio, Gaetano Serviddio and Gianluigi Vendemiale
Antioxidants 2025, 14(6), 656; https://doi.org/10.3390/antiox14060656 (registering DOI) - 29 May 2025
Abstract
Redox imbalance plays a pivotal role in the regulation of inflammation, influencing both the onset and progression of various inflammatory conditions. While the pro-inflammatory role of oxidative stress (OS) is well established, the impact of reductive stress (RS)—a condition marked by excessive reducing [...] Read more.
Redox imbalance plays a pivotal role in the regulation of inflammation, influencing both the onset and progression of various inflammatory conditions. While the pro-inflammatory role of oxidative stress (OS) is well established, the impact of reductive stress (RS)—a condition marked by excessive reducing equivalents such as NADH, NADPH, and reduced glutathione (GSH)—remains underappreciated. This review offers a novel integrative perspective by analyzing how OS and RS act not merely in opposition, but as interconnected modulators of immune function. We explore the mechanisms through which OS activates inflammatory pathways, and how RS, when sustained, can paradoxically impair immune defense, alter redox-sensitive signaling, and contribute to disease progression. Emphasis is placed on the dynamic interplay between these redox extremes and their combined contribution to the pathogenesis of chronic inflammatory diseases, including autoimmune, cardiovascular, and neuroinflammatory disorders. Additionally, we evaluate therapeutic strategies that target redox homeostasis, arguing for a shift from antioxidant-centric treatments to approaches that consider the bidirectional nature of redox dysregulation. This framework may inform the development of more precise interventions for inflammation-related diseases. Full article
(This article belongs to the Special Issue Redox Regulation in Inflammation and Disease—3rd Edition)
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